Plaque and Calculus

Composition, Development, and Its

Relationship to Disease

What Is Plaque?
An invisible layer of microorganisms growing
in a colony on the teeth
Specific bacteria in the colony are the etiology
of dental caries and periodontal diseases
Plaque begins to form immediately on a freshly
polished tooth, but it takes approximately 21
days for plaque to completely mature
If plaque is disturbed (brushed away) when it
begins to form, it does not mature

What Is Plaques Composition?

Plaque is composed of:
Components of saliva (glycoproteins)
Various bacterium including gram + and
gram -; aerobic, facultative, and anaerobic;
saccharolytic (metabolize sugars) and
asaccharolytic (dont require sugars)
Bacteria metabolism products
Minerals and their ions (ca+, PO4, F )

Is This Plaque?

Is This Plaque?
Arrow points to visible
material so its not plaque, its
materia alba
Materia alba is food debris,
dead cells, bacteria
plaque is underneath
materia alba

What Damage Plaque Can Do

Plaque requires stain

to be seen because it is
invisible

THIS IS PLAQUE!

From healthy

To localized
(30% or less)

To generalized
(75% or more)

More Damage
TOOTH
GINGIVA

CEJ

BONE

From treatable--

PDL

To hopeless

A Freshly Polished Molar

SULCUS

SULCULAR EPITHELIUM
ATTACHMENT
LAMINA PROPRIA
(Connective tissue)

In minutes salivary
glycoproteins form the
acquired pellicle on ALL
teeth. (Its that slick
f li on your teeth)
feeling
t th)
The part of pellicle that
attaches to tooth
irregularities is called
subsurface pellicle
Pellicle itself is acellular

PDL
BONE

A Molar Within 24 Hours That

Is Not Brushed
In 24 hours aerobic,
gram + bacteria
(primary colonizers)
such as streptococcus
sanguis,
i s. mutans,
t
Rothia, Actinomycosis
begin growing in pellicle
Neisseria, gram
facultative anaerobe also
primary colonizer

Stem cells in bone marrow

produce inflammation
and immunity cells and
send them to body tissues
blood
for later use

Stem cell

Thymus
T Lymphocyte

blood
Lymph tissue

PMN

Monocyte

B
Lymphocyte

Macrophage
In
tissue

Initial gingivitis

A Molar Not Brushed For 24 Hours

If bacteria are allowed to
grow, there is an
immediate subclinical
inflammatory response
(
(cant
t b
be seen clinically)
li i ll )
PMNs (neutrophils)
enter lamina propria
pmn pmn
pmn

Initial gingivitis

A Molar Not Brushed in 2-3 Days

Secondary colonizers such
as Provetella, intermedia,
capnocytophaga series,
fusobacterium nucleatum,
and bacteriodes
i
forsyth
f
such as begin growing
Inflammation still acute
and subclinical but blood
vessels beginning to dilate,
macrophages appear,
pmns move into junctional
epithelium, sulcus

pmn
pmn
macrophages

pmn

Initial gingivitis

A Molar within 4-6 Days That

Is Not Brushed
Plaque becoming thicker,
tertiary colonizers such as
A.A., P. gingivalis, treponema
d ti l campylobacter
denticola,
l b t
recta appear
Endotoxins from gram
bacteria begin to form)
Now considered EARLY
(STAGE TWO) GINGIVITIS

A Molar within 4-6 Days That

Is Not Brushed
ulcers appear in sulcular
epithelium,
signs of inflammation
may begin to be clinically
apparent (bleeding
apparent,
(bleeding,
slight redness, swelling)
Lymphocytes become the
most prolific WBC, a sign
of chronic inflammation

lymphocytes

lymphocytes

Early gingivitis

A Molar Not Brushed for 7-14 Days

Plaque grows apically,
thickens
Inflammatory
response intensifies
Crystal niduss of
minerals (calcium,
phosphates, etc) grow
together to form
calculus
Early gingivitis

lymphocytes
lymphocytes

macrophages

pmn

A Molar Not Brushed for 14-21 Days

Piles of bacteria form
domes, corncobs,
test tube brushes
present
Plasma cells, mast cells,
macrophages
p g increase in
connective tissue
Plaque has matured
Bacterial biproducts
(colleganase, protease)
now ready to break
down attachment and
cause it to migrate
apically

Domes

lymphocytes
lymphocytes

Plasma cell

pmn
pmn
pmn

pmn
pmn

Mast cell

macrophage

Established gingivitis

Plaque and Periodontal Disease

When attachment
migrates apically, it is no
longer gingivitis but
periodontitis
Most common form is
chronic periodontitis
Contributing factors can
alter or intensify process
but its pathogenesis
stays the same

Attachment
migrated apically

Plaque and Periodontal Disease

Unattached plaque has more
motile, gram bacteria with
many WBCs
TISAP has gram -, motile
bacteria that invade tissue
through ulcers in sulcular
epithelium

TOOAP

unattached
TISAP

How Bone and the PDL Are

Destroyed
The inflammatory process
spreads to PDL.
Sharpeys
p y fibers are
destroyed by collagenase
and protease
Endotoxins are
incorporated into
cementum

Plaque and Periodontal Disease

Subgingival plaque is tooth

associated (TOOAP),
unattached, and tissue
associated (TISAP)
TOOAP is continuation of
supragingival plaque, has more
gram +, nonmotile bacteria in
coronal 1/3, more gram -, motile
bacteria in apical 1/3

TOOAP

unattached
TISAP

How Bone and the PDL Are

Destroyed
Gram bacteria endotoxins
enter lamina propria
through ulcers in
epithelium
They follow vascular
bundles to bone where they
stimulate osteoclasts to
destroy bone

Different Patterns of Destruction

Horizontal bone loss
Vertical bone loss
Buccal bone loss

What is Calculus?
Calculus is
mineralized plaque
Calculus is a
contributing factor to
dental diseases
Calculus provides a
rough surface on
which bacterial plaque
can grow

How Does Calculus Attach?

Attaches three ways
Irregularities
Cohesion
Acquired pellicle

Supragingival vs Subgingival
Calculus
Supragingival
Minerals come from
saliva
Usually whitish in
color
Found mainly near
salivary ducts

Subgingival
Minerals come from
sulcular fluids
Usually black in color
Found everywhere